Taenia infestations are caused by parasitic flatworms (cestodes) that have complex life cycles involving an intermediate and definitive host. The most common types that infect humans are Taenia saginata and Taenia solium. T. saginata uses cattle as the intermediate host and humans as the definitive host, causing beef tapeworm infection. T. solium uses pigs and sometimes humans as intermediate hosts, and humans as the definitive host, causing both pork tapeworm infection and the potentially serious condition of cysticercosis when ingested eggs develop into cysticerci larvae in tissues. Symptoms depend on the location of the cysticerci but can include seizures, headaches, and hydrocephalus if in
4. Cestodes
• Flattened, ribbon-like, without body cavity.
• Head, neck and segmented strobilus.
• Head : suckers, rostellum and hooklets .
• Neck : budding zone from which segments are formed.
• Strobilus : immature, mature and gravid proglottids.
• Hermaphrodites
• Digestive tract : absent, nutrition is absorbed by villi
of body surface.
5. • Complex two-host life cycle
• Human beings are the only definitive host
• Intermediate hosts can be pigs, cattle and also
human being
• Most common in Latin America, Africa and
India
6. Taenia saginata
• Also called beef tapeworm
• Word wide, highest prevalence (up to 27%)
are in central Asia, the Near East, and Central
and East Africa.
• Habitat: upper jejunum of man
• Definitive host : human
• Intermediate host : cattle's
8. Morphology
• Adult : scolex, neck and strobila
• Length : 2-5m but can reach upto 10m
• Scolex : large, quadrate, four suckers without
rostellum and hooklets
• Neck : active structure from which proglottids
are continuously formed
• Body(strobila) : chain of proglottdis
9. • Proglottids : each 20x5mm in breadth and
length,
• 1000-2000 in numbers
• Motile
• Expelled singly
• No. of lateral branches of uterus 15-30
• Also contains vagina, testes ovary
12. Eggs
• Spherical, brown in colour
• 31-43µm in diameter
• Surrounded by embryophore
• Inside the emryophore is the hexacanth
embryo(oncosphere) with three pairs of
hooklets
• Does not float on saturated salt solution
• Infective only to cattles
15. Pathogenesis
• Adult tapeworms : minimal local pathology
• Vague abdominal discomfort, indigestion,
diarrhoea, constipation, loss of appetite
• An immune response to adult tapeworms
provokes eosinophilia and immunoglobulin
E(IgE) elevation in some patients
16. Diagnosis
• Detection of egg and proglottid in stool
• Direct stool smear or by sedimentation
technique
• Egg do not float on saturated salt solution
• Anal swab is superior method
• Eggs of T. saginata and T. soluim are very
similar
17. • Proglottids morphlogy and structure are used
to differentiate between the two type of
taenia
• Scolex structure can also be used
18. Treatment
• Single dose of praziquentel 10mg/kg is highly
effective
• Niclosamide single 2gm single dose is also
effective
19. Prophylaxis
• Inspection of all beef for cysticerci bovis
• Thorough cooking
• Proper disposal of faeces
• Infected people should be treated to break
parasitic life cycle
20. Taenia solium
• Also called pork tapeworm
• T. solium infection is endemic include Mexico,
Central America, South America, Africa,
Southeast Asia, India, the Philippines, and
southern Europe.
• definitive host : human
• Intermediate host : pigs or human
21. Morphology
• Adult : scolex, neck and strobila
• Length : 2-4m
• Scolex : small, globular, four suckers with
rostellum and a double row of hooklets
• Neck : active structure from which proglottids
are continuously formed
• Body(strobila) : chain of proglottdis
22. • Proglottids : each 12x6 mm
• 800-1000 in numbers
• Non motile
• Expelled in small chains of 5 or 6
• No. of lateral branches of uterus 5-10
• Also contains vagina, testes ovary
• Eggs are similar to that of T. saginata and it
can also infect human causing cystercosis
24. Pathogenesis
• Similar to that of T. saginata
• But humans can also get infected by the egg
through autoinfection
• Autoinfection occurs by oro fecal route due to
poor hygiene and also by reverse peristalsis
• Infection by egg leads to cysticercocis
25. • Diagnosis of intestinal infection with T. solium
is similar to that of T. saginata with egg in
stool and species differentiation with
proglotid and scolex
• All cases of diagnose intetinal T. solium should
be examined for cysticercosis
26. Treatment
• Praziquentel 10mg/kg single dose is the drug
of choice
• Niclosamide single 2gm single
• Vomiting should be avoided to prevent
cysticercosis
• Puragtives may be given 1-2 hr after
antihelminthic treatment
• Instructed for carefull washing of both hands
after defecation
27. Prophylaxis
• Personal hygiene
• Sanitory measures
• Strict inspectuion of pork in slaughter huose
• Thorough cooking
• Proper disposal of human faeces
• Avoid eating raw vegetables grown on soil
irrigated by sewage water
• Treatment of infected person
28. Cysticercosis
• Cysticercosis is a disease caused by the
presence of cysticercus cellulosae and
cysticercus racemose, the larval forms of T.
solium in dfferent tissues
• A major cause of adult-onset epilepsy in the
developing world.
29. Target tissue
• Predilection for migration to eyes, CNS and
striated muscles.
• CNS involvement is termed as
Neurocysticercosis
30. Types of cysts
Cysticercus cellulosae
• Larva form of T. solium in host tissue
• Small (<2cm), round, thin walled
• Lodges in the parenchyma or the
subarachnoid space
• Provokes only a minor inflammation
• Often remain silent
31.
32. Cysticercus racemose
• Large lobulated cysts with predilection for basal
cisterns
• Causes cysticercotic arachnoiditis and presents as
meningitis
• Causes obstruction of 4th ventricle and resultant
raised ICP and hydrocephalus
• Can cause occlusion of vessels and vasculits
resulting in stroke
• Causes intense inflammatory reaction and
seizures
34. Mode of infection
• Humans are both intermediate and definitive
hosts.
• Cysticercosis develops when humans become
intermediate hosts by ingesting the
embryonated eggs of the tapeworm, which
release oncospheres that penetrate the
intestinal wall, enter the bloodstream, and
disseminate into the tissue.
35. • HETEROINOCULATION
– eggs may come from the environment
• INTERNAL AUTOINOCULATION
– regurgitated from proglottids into the stomach
• EXTERNAL AUTOINOCULATION
– from the fingers of an infected person
38. Presentation
• The clinical presentation of NC is determined
by
• Location of cysts
• Size of cysts
• Cyst load (number of cysts)
• Host’s immune response
41. • Intraventricular NC
– 5- 10% of all cases
– 4th ventricle most common site for obstruction
– Cysts in lateral ventricles less likely to cause
obstruction
– Hydrocephalus and acute, subacute or
intermittent signs of raised ICP without localizing
signs
42.
43. • Meningeal NC
– Meningeal irritation resembling TBM
– Raised ICP from oedema, inflammation and
presence of cyst obstructing flow of CSF
45. Investigations
• Stool Routine and Microscopy
• Fundoscopy
• Biopsy and histopathology
• CT with contrast
• MRI
• Serology
– EITB
• sensitivity of 98% specificity of 100%
– ELISA in CSF
• sensitivity of 87% specificity of 95
46. Diagnostic Criteria for Human
Cysticercosisa
• 1. Absolute criteria
a. Demonstration of cysticerci by histologic or microscopic examination of biopsy
material
b. Visualization of the parasite in the eye by funduscopy
c. Neuroradiologic demonstration of cystic lesions containing a characteristic scolex
• 2. Major criteria
a. Neuroradiologic lesions suggestive of neurocysticercosis
b. Demonstration of antibodies to cysticerci in serum by enzyme-linked
immunoelectrotransfer blot
c. Resolution of intracranial cystic lesions spontaneously or after therapy with
albendazole or praziquantel alone
• 3. Minor criteria
a. Lesions compatible with neurocysticercosis detected by neuroimaging studies
b. Clinical manifestations suggestive of neurocysticercosis
c. Demonstration of antibodies to cysticerci or cysticercal antigen in cerebrospinal fluid
by ELISA
d. Evidence of cysticercosis outside the central nervous system (e.g., cigar-shaped soft-
tissue calcifications)
• 4. Epidemiologic criteria
a. Residence in a cysticercosis-endemic area
b. Frequent travel to a cysticercosis-endemic area
c. Household contact with an individual infected with Taenia solium
47. Diagnosis
• Definitive
a. 1 absolute
b. 2 major + 1 minor + 1 epidemiological
• Probable
a. 1 major + 2 minor
b. 1 major + 1 minor + 1 epidemiological
c. 3 minor + 1 epidemiological
48. Tuberculoma Versus Cysticercus
Granuloma
Cysticercus Granuloma
• Round in shape
• Cystic
• 20mm or less with ring
enhancement or visible
scolex
• Cerebral edema not
enough to produce
midline shift or focal
neurological deficit
Tuberculoma
• Irregular in shape
• Solid
• Greater than 20mm
• Associated with severe
perifocal edema and
focal neurological
deficit
49. Natural course
• Rate of spontaneous resolution of a solitary
cysticercus granuloma in patients with
seizures
• 3 months - 18.8%
• 6 months - 36.4%
• 1 year - 62.5%
50. Treatment
• Antiepileptic therapy
• corticosteroids (dexamethasone)
• albendazole (15 mg/kg per day for 8–28 days)
or praziquantel (50–100 mg/kg daily in three
divided doses for 15–30 days).
51. Steroids
• Corticosteroids represent the primary form of
therapy for cysticercal encephalitis and
arachnoiditis causing hydrocephalus and
progressive entrapment of cranial nerves.
• High doses of iv Dexamethasone can be
followed by oral therapy with Prednisolone
1mg/kg/day or Dexamethasone 0.1mg/kg/day
administered 3 times a week
52. • glucocorticoids induce first-pass metabolism
of praziquantel and may decrease its
antiparasitic effect
• cimetidine should be co-administered to
inhibit praziquantel metabolism
• For this reason albendazole is preferred
53. Surgery restricted to
• Placement of ventriculo-peritoneal shunts for
hydrocephalus
• Excision of single big cysts causing mass effect
• Endoscopical excision of intraventricular
parasites.
54. Recommendation
• Individualize therapeutic decisions, including
whether to use antiparasitic drugs, based on
the number, location, and viability of the
parasites within the nervous system;
• Actively manage growing cysticerci either with
antiparasitic drugs or surgical excision;
55. • Prioritize the management of intracranial
hypertension secondary to neurocysticercosis
before considering any other form of therapy;
and
• Manage seizures as done for seizures due to
other causes of secondary seizures (remote
symptomatic seizures) because they are due to
an organic focus that has been present for a long
time
56. • Treatment with albendazole plus antiepileptic drugs
has no benefit over treatment with antiepileptic drugs
alone.
• Albendazole treatment may cause problems or have
adverse effects with regard to increased seizure
frequency, encephalopathy and hospital readmissions
in the early part of the treatment.
• Albendazole treatment may be disadvantageous from
an economical perspective because of the direct and
indirect treatment costs and the loss of working days
57. Uncummon taenia
• Taenia saginata asiatica : closely related to T.
saginata with pig as intermediate host
• Taenia crassiceps cysticercosis : Rodents are
the preferred host but rare human infections
have been reported, most recently in
association with AIDS.
• Taenia multiceps is a parasite of dogs, with
sheep being the principal intermediate host.
Larva is called coenurus.